610株大肠埃希菌对抗菌药物的敏感性分析

目的 探讨大肠埃希菌(ECO)的耐药现状,为临床医师合理用药提供科学参考依据.方法 严格按照《全国临床检验操作规程》对610株ECO进行培养、鉴定；采用K-B法检测ECO对抗菌药物的敏感性,并根据CLSI2009年折点判断结果.结果 ECO检出率最高的科室是神经内科和ICU,分别占25.9％、21.3％;610株ECO中ESBLs阳性207株,阳性率33.9％,产与非产ESBLs菌株均对亚胺培南及美罗培南100.0％敏感.结论 临床医师应根据药敏结果合理选用抗菌药物,以提高临床治愈率.     

产超广谱β-内酰胺酶大肠埃希菌感染分布及危险因素分析

目的分析近两年来深圳市第三人民医院产超广谱β-内酰胺酶(ESBLs)-大肠埃希菌(ECO)的来源标本类型、病区分布,以及危险因素,为医院感控和临床抗感染治疗提供细菌学依据。方法收集该院住院患者检出的非重复ECO 443株,采用phoenix100系统进行菌种鉴定和药敏实验,并对产ESBLs-ECO进行双纸片协同试验确证,对产ESBLs-ECO感染的危险因素进行统计分析。结果 443株ECO中产ESBLs-ECO为115株,占26.0%;产ESBLs-ECO菌株主要分离自痰液、尿液和血液标本,病区分布以结核病区、儿科、肝病区和感染科为主,分别占20.9%、13.9%、12.2%和8.7%。男性、外科手术和第三代头孢菌素用药史是产ESBLs-ECO感染的独立危险因素。结论该院产ESBLs-ECO检出率较高,医院应根据危险因素制订干预措施,特别应重点关注男性患者,规范外科手术操作及消毒,限制使用第三代头孢菌素,减少院内产ESBLs-ECO的发生和传播。     

Occurrence of Extended-Spectrum Betalactamases (ESBL) in Dutch Hospitals

Summary The prevalence of ESBL was determined among isolates of Escherichia coli (n = 571) and Klebsiella spp. (n = 196) collected during a 1-week study period in 8 university and 3 large regional laboratories all over the Netherlands. 18 isolates were positive for at least one of the screening tests used, i.e., VITEK-ESBL, E-test ESBL and MIC ratio of ceftazidime/ceftazidime-clavulanic acid, cefotaxime/cefotaxime-clavulanic acid. In 5 of these 18 putative ESBLs no betalactamase production was detectable. A TEM type was found in three E. coli and two Klebsiella spp. An SHV type was present in five Klebsiella spp. In one E. coli and one Klebsiella pneumoniae both enzymes were present. In one Klebsiella oxytoca neither of the two enzymes was present. Using PCR for both ESBL TEM and ESBL SHV, an SHV ESBL was found in one E. coli and four Klebsiella isolates. The mutations at position 238 and 240 were already described. In one E. coli isolate a TEM ESBL was found with three mutations, at position 21, 164 and 265. These mutations were already described in other ESBLs but not in this combination suggesting a new TEM ESBL. The overall prevalence of ESBL producing E. coli and Klebsiella spp. was less than 1% (6 out of 767). Received: December 14, 1998 · Accepted: September 19, 1999     

产ESBLs大肠埃希菌和肺炎克雷伯菌的分布及耐药分析

目的：探究产ESBLs大肠埃希菌和肺炎克雷伯菌的分布和耐药性。方法对2013年6月—2014年6月该院住院患者送检的标本进行培养,采用VITEK细菌鉴定与药敏分析系统行菌种鉴定和药敏分析,对产ESBLs大肠埃希菌和肺炎克雷伯菌的临床分布和耐药性进行分析。结果产ESBLs大肠埃希菌和肺炎克雷伯菌主要从尿液45.94%、痰液85.29%中检出;产ESBLs菌对碳青霉烯类、阿米卡星等药物敏感性较高耐药率1.47%~22.19%。结论产ESBLs大肠埃希菌和肺炎克雷伯菌主要引起泌尿道和下呼吸道感染,并对大部分常用抗菌药物耐药。     

ICU产ESBLs大肠埃希菌和肺炎克雷伯菌耐药性分析

目的探讨医院重症监护病房产超广谱β-内酰胺酶(ESBLs)大肠埃希菌和肺炎克雷伯菌的耐药性。方法采用BD Phoenix100全自动微生物分析仪对莒县中医医院重症监护病房产超广谱β-内酰胺酶(ESBLs)大肠埃希菌和肺炎克雷伯菌进行细菌鉴定和药物敏感试验。结果产ESBLs大肠埃希菌和肺炎克雷伯菌均呈现多重耐药,大肠埃希菌对亚胺培南、哌拉西林/他唑巴坦和阿米卡星的耐药率分别为1.8%、5.5%和20.0%,其余14种抗生素的耐药率在54.6%~100.0%;肺炎克雷伯菌对亚胺培南无耐药现象,其余16种抗生素的耐药率在56.0%~100.0%。结论重症监护病房分离的产ESBLs大肠埃希菌和肺炎克雷伯菌多重耐药严重;同样是产ESBLs菌株,大肠埃希菌和肺炎克雷伯菌对相同抗生素的敏感率明显不同。     

Treatment strategies for central nervous system infections: an update

Introduction: Central nervous system infection continues to be an important cause of mortality and morbidity worldwide. Our incomplete knowledge on the pathogenesis of how meningitis-causing pathogens cause CNS infection and emergence of antimicrobial resistance has contributed to the mortality and morbidity. An early empiric antibiotic treatment is critical for the management of patients with bacterial meningitis, but early recognition of bacterial meningitis continues to be a challenge.

Areas covered: This review gives an overview on current therapeutic strategies for CNS infection with a focus on recent literature since 2010 on bacterial meningitis. Bacterial meningitis is a medical emergency, requiring early recognition and treatment. The selection of appropriate empiric antimicrobial regimen, after incorporating the epidemiology of bacterial meningitis, impact of vaccination, emergence of antimicrobial-resistant bacteria, role of adjunctive therapy and the current knowledge on the pathogenesis of meningitis and associated neuronal injury are covered.

Expert opinion: Prompt treatment of bacterial meningitis with an appropriate antibiotic is essential. Optimal antimicrobial treatment of bacterial meningitis requires bactericidal agents able to penetrate the blood–brain barrier, with efficacy in cerebrospinal fluid. Emergence of CNS-infecting pathogens with resistance to conventional antibiotics has been increasingly recognized, but development of new antibiotics has been limited. More complete understanding of the microbial and host factors that are involved in the pathogenesis of bacterial meningitis and associated neurologic sequelae is likely to help in developing new strategies for the prevention and therapy of bacterial meningitis.     

Upregulation of Shiga Toxin Receptor CD77/Gb3 and Interleukin‐1β Expression in the Brain of EHEC Patients with Hemolytic Uremic Syndrome and Neurologic Symptoms

In 2011, a large outbreak of Shiga toxin‐producing enterohemorrhagic Escherichia coli (EHEC) infections occurred in northern Germany, which mainly affected adults. Out of 3842 patients, 104 experienced a complicated course comprising hemolytic uremic syndrome and neurological complications, including cognitive impairment, aphasia, seizures and coma. T2 hyperintensities on magnet resonance imaging (MRI) bilateral in the thalami and in the dorsal pons were found suggestive of a metabolic toxic effect. Five of the 104 patients died because of toxic heart failure. In the present study, the post‐mortem neuropathological findings of the five EHEC patients are described. Histological investigation of 13 brain regions (frontal, temporal, occipital cortex, corpora mammillaria, thalamus, frontal operculum, corona radiata, gyrus angularis, pons, medulla oblongata, cerebellar vermis and cerebellar hemisphere) showed no thrombosis, ischemic changes or fresh infarctions. Further, no changes were found in electron microscopy. In comparison with five age‐matched controls, slightly increased activation of microglia and a higher neuronal expression of interleukin‐1β and of Shiga toxin receptor CD77/globotriaosylceramide 3 was observed. The findings were confirmed by Western blot analyses. It is suggested that CD77/globotriaosylceramide upregulation may be a consequence to Shiga toxin exposure, whereas increased interleukin‐1β expression may point to activation of inflammatory cascades.     

Escherichia coli O121:H19 infection identified on microagglutination assay and PCR

Non‐O157 Shiga toxin‐producing Escherichia coli (STEC) strains are increasingly recognized as foodborne pathogens that trigger hemolytic uremic syndrome (HUS). The detection and isolation of these strains is important, but distinguishing their bacteriological profiles is difficult. A 2‐year‐old girl developed HUS with mild renal involvement 22 days after consuming barbecued meat. Clinical and laboratory findings gradually improved without specific treatment. Because neither enterohemorrhagic E. coli (EHEC) nor Shiga toxins were detected in stool cultures in a clinical laboratory and the patient tested negative for circulating antibodies to O157 lipopolysaccharide, the case was initially diagnosed as probable atypical HUS. Subsequent serodiagnostic microagglutination assay and polymerase chain reaction‐based molecular testing, however, indicated the presence of the EHEC O121:H19 strain with stx2. Thus, to correctly diagnose and treat HUS, a system for detecting non‐O157 STEC in a clinical setting is urgently needed.     

大肠杆菌K1穿越血脑屏障机制研究进展

新生儿化脓性脑膜炎是一种危重的中枢神经系统感染性疾病.大肠杆菌K1菌株(Escherichia coli K1,Ecoli K1)是常见的导致新生儿化脓性脑膜炎的革兰阴性菌,大部分大肠杆菌脑膜炎是血源性传播所导致,其穿过血脑屏障(blood-brain barrier,BBB)的机制一直是研究的重点.相关研究表明,Ecoli K1穿越BBB与高水平菌血症、对脑微血管内皮细胞的侵袭、受体介导的胞吞转运、活菌穿越BBB密切相关.该文从上述四个方面对E.coli K1穿过BBB进入大脑引起新生儿化脓性脑膜炎的发病机制进行综述.     

Molecular characterization of diarrheagenic Escherichia coli pathotypes: Association of virulent genes,serogroups, and antibiotic resistance among moderate‐to‐severe diarrhea patients

Background

Diarrheagenic Escherichia coli (DEC) signifies as an important etiological agent of moderate‐to‐severe diarrhea. This study was primarily focused on molecular identification of DEC pathotypes; their association with serogroups and estimates of resistance profiles against different antibiotics regime.

Methods

Five hundred seventy‐two stool specimens from diarrhea patients were investigated for DEC pathotypes. Molecular pathotypes were identified by amplification of virulence genes associated with distinct pathotypes followed by sequencing. Diarrhea is a self‐limiting disease, however, severity and persistence of infection suggest antibiotic use. Therefore, AST and MIC were determined against common antibiotic regimen. Correlations between molecular pathotypes and serogroups were analyzed by somatic “O” antigen serotyping.

Results

The present findings reveal incidence of DEC as an etiological agent up to a level of 21% among all diarrheal age groups. DEC infection rate was higher in children. Enteropathogenic E. coliEPEC, a molecular pathotype of DEC, was found as a predominant pathotype with highest frequency of 13.7%. Two other molecular pathotypes enterotoxigenic E. coli (ETEC) and enteroaggregative E. coli (EAEC) accounted for 5.7% and 1.3%, respectively for all diarrhea incidences. Serological analysis deciphered somatic antigens O26, O2, and O3 as major serogroups identified among EPEC, ETEC, and EAEC pathotypes, respectively. All DEC pathotypes exhibited high levels of antibiotic resistance except for cotrimoxazole and norfloxacin.

Conclusion

Comprehensive molecular characterization of DEC pathotypes, their incidence estimates, and antibiogram patterns will help in ascertaining better diagnostic and therapeutic measures in management of diarrheal diseases.